Short cases in medicine

Short cases in medicine
Cardiovascular system
Examination routine
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Introduce yourself and take consent
Ensure adequate exposure and request for a
chaperone if neccessary
Proper positioning of the patient at 45 degrees
Comment on the general appearance of the patient
especially whether he or she is dyspnoeic or ill
looking
Start with the general examination
Febrile/not
Marfanoid features
Conjunctivae for pallor
Central and peripheral cyanosis
Dental hygiene
Finger and toe clubbing
Peripheral stigmata of infective endocarditis
Ankle edema/ sacral edema
Outline of CVS Examination
General examination
Pulse examination
Blood pressure
Precordial examination
Inspection
Palpation
Auscultation
Lung bases
Liver
Then move on to the examination of the pulses. This is divided into arterial pulse examination
and examination of the jugular venous pulse
Arterial pulse examination
Start with the radial pulse and assess the rate and the rhythm
Look for the character of the pulse and examine for collapsing pulse
Examine the peripheral pulses quickly and then go on to look for radio-radial or radio-femoral
delay
Look at the neck for visible carotid pulses
Feel the carotid pulse and comment on the volume of the pulse
Examine the jugular venous pulse
Try to look for the waveform of the JVP and measure the height of the venous pressure in
centimeters
Offer to measure the blood pressure
Examine the precordium
Inspection
Look for any chest deformities
Surgical scars- especially midline sternotomy scars and left thoracotomy scars
Look for visible pulsations over the chest wall
Palpation
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Palpate for the apex beat and comment on the position of the apex beat and whether it is
displaced or not. Also comment on the character of the apex beat
Palpate for thrills over the precordium
Palpate for a left parasternal heave which is indicative of right ventricular hypertrophy
Look for a palpable 2nd heart sound in the pulmonary area which is suggestive of pulmonary
hypertension
Auscultation
Listen to the heart sounds first and comment on any abnormality
Auscultate in all 4 areas
Remember to demonstrate auscultation in the mitral area with the bell and the patient in the
left lateral position for the murmur of mitral stenosis.
Examine the patient seated and leaning forward with the breath held in expiration for the
murmur of aortic regurgitation
Listen for any murmur and describe the murmur based on the following points. Always
remember to show the examiner that you are timing the murmur by palpating the carotid
pulse (R side)
Systolic or diastolic
Further as pan systolic, mid systolic, early diastolic etc.
The location where the murmur is best heard
The grade of the murmur
Radiation of the murmur
The effect of respiration on the murmur (Remember that the intensity of all right sided murmurs
is increased with inspiration and the intensity of all left sided murmurs are increased with
expiration)
Examine the liver and lung bases for evidence of cardiac failure
Try to reach a diagnosis before auscultation. This is possible and is extremely helpful for those who are
not that good in auscultation. Study the following table.
Mitral stenosis
What is the diagnosis?
Why do you say so? What are the
other lesions which could present
with similar clinical findings?
Remember that the lesions given below are
extremely rare and are never given for the exam.
But the above question is a very popular one.
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Carey Coombs murmur in acute
rheumatic carditis
Austin flint murmur in severe aortic
regurgitation
Atrial myxoma
What is the most probable aetiology?
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Mitral stenosis is almost always rheumatic in origin
How would you clinically determine the severity of the lesion from the findings
of the physical examination?
The following are some features which would indicate a severe lesion
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Longer the murmur the more severe the stenosis
The gap between the second sound and the opening snap (a narrow gap would indicate severe
stenosis but the opposite is not true)
Evidence of complications
Atrial fibrillation
Pulmonary hypertension
What are the complications associated with mitral stenosis?
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Left atrial dilatation and atrial fibrillation
Left atrial thrombus +/- systemic
embolization
Pulmonary hypertension
Tricuspid regurgitation
Right heart failure
What are the investigations you would like to perform on this patient?
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ECG – P mitrale
CXR – Enlarged left atrial appendage and pulmonary
congestion
Echo – This is the most important investigation. It
confirms the diagnosis and looks for other associated
valvular lesions. It also estimates the severity of the
lesion based on the valve surface area and pressure
gradient across the mitral valve. Echo is also useful to
decide the mode of intervention
How would you manage this patient?
Medical management
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Management of atrial fibrillation
Interventional management
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Consider the following indications for
intervention in a patient with mitral
stenosis
Symptomatic patients with significant
mitral valve stenosis
Patients with pulmonary
hypertension even if minimally
symptomatic
The options available for
management are PTMC
(percutaneous trans-septal mitral
valve comissurectomy) and valve
replacement
PTMC is a less invasive method but
requires the following
Isolated MS (no evidence of valvular
regurgitation)
Mitral valve should be mobile and
pliable
Left atrium free of thrombus
Mitral regurgitation
What is the diagnosis?
What are the possible causes you would consider for this condition?
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The causes for mitral regurgitation
can be classified as acute and chronic
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Acute
Acute myocardial infarction
Infective endocarditis
Acute rheumatic carditis
Chronic
Mitral valve prolapse
Rheumatic heart disease
Cardiomyopathy
How would you clinically assess the severity of the lesion?
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Degree of left ventricular dilation
Evidence of complications – heart failure
What are the investigations you would like to perform in this patient?
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ECG – P mitrale left ventricular hypertrophy, atrial fibrillation. Remember that if myocardial
infarction is the aetiology there will be evidence of an old infarct
CXR – Enlarged left atrium and ventricle with evidence of pulmonary congestion
Echocardiogram confirms the diagnosis, establishes the anatomy and function of the mitral
valve and assesses the severity of the lesion
How would you manage this patient?
Medical management
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Management of atrial fibrillation
Management of heart failure
Surgical intervention
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The following are general indications for surgical intervention
Severe acute mitral regurgitation
Severe symptomatic chronic MR (symptoms are described based on the NYHA classification)
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Asymptomatic chronic MR with evidence of progressive dilation of the left ventricle and
deterioration of the ejection fraction
Options available are mitral valve repair and mitral valve replacement
Aortic stenosis
What is the diagnosis?
What are the other lesions which can present with similar physical signs?
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Aortic sclerosis may be confused with aortic stenosis
Aortic sclerosis affects the elderly. On examination the pulse volume is normal and the murmur
is more localized
What is the probable aetiology you would
consider?
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Remember that the aetiology of aortic stenosis
varies according to the age of the patient
In adolescents the lesion could be congenital
Young adults and middle aged individuals
Calcification of a bicuspid aortic valve
Rheumatic heart disease
Middle aged to elderly
Senile degenerative aortic stenosis
Rheumatic heart disease
Calcification of a bicuspid aortic valve
How would you clinically determine the severity of the lesion?
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Narrow pulse pressure
Narrow or reverse split second heart sound
Clinical evidence of heart failure
What are the investigations you would like to perform on this patient?
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ECG – Left ventricular hypertrophy, ST segment depression and T wave inversion in advanced
cases
CXR
Echocardiogram
This investigation confirms the diagnosis and assesses the severity of the lesion based on valve
surface area and pressure gradient across the aortic valve
How would you manage this patient?
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Immediate intervention is recommended in patients with AS who develop symptoms – angina,
shortness of breath, syncopal attacks as the lesion progresses rapidly to cause cardiac failure
Asymptomatic patients with severe aortic stenosis
Valve replacement is the treatment of choice
Aortic regurgitation
What is the diagnosis?
What are the signs you would look for in the general examination if you are
suspecting the above diagnosis?
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The general examination will reveal special signs associated with AR and also give clues to the
aetiology of the condition
Head nodding (de Musset’s sign)
Visible carotid pulsations (Corrigan’s sign)
Capillary pulsations (Quincke’s sign)
Pistol shot femorals
Look for features of Marfan’s syndrome – high
arched palate, arachnodactyly, arm span greater
than height
Examination of the pupils for Argyll Robertson
pupil which is seen in syphilis
Examine the joints and back for rheumatoid
arthritis and ankylosing spondylitis
The diagram demonstrates the signs associated with Marfan’s syndrome
What is the probable aetiology you would consider for this lesion?
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Congenital abnormality of the aortic valve
cusps
Acquired
Rheumatic heart disease
Infective endocarditis
Trauma
Aortic root dilation in – Marfan’s syndrome,
aortic dissection, syphilis, seronegative
arthritis (ankylosing spondylitis), rheumatoid
arthritis
How would you clinically assess the
severity of the lesion?
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The duration and intensity of the murmur – a longer and louder murmur indicates a severe
lesion
Presence of the Austin Flint murmur (MDM heard at the apex)
Wide pulse pressure
Features of left ventricular failure
What are the investigations you would like to perform in this patient?
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ECG – May show left ventricular hypertrophy in advanced cases
CXR – left ventricular dilation and aortic root dilation in certain cases
Echocardiogram
This is the investigation of choice for the confirmation of the diagnosis. It also assesses the
severity of the lesion and may indicate an aetiology
How would you manage this patient?
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Medical management
Manage heart failure and any associated co morbidities
Surgical management with valve replacement should be considered in the following
circumstances
Acute AR
Symptomatic patients
Asymptomatic patients with progressively increasing ventricular dilation and declining left
ventricular function
Mixed valve disease
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The most common combination given for the exam is mixed mitral valve disease. If such a case is
encountered in the exam it is important to state which lesion is prominent
Ventricular septal defect
What is the diagnosis?
What are the other lesions which
can present with similar clinical
signs?
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The murmur of tricuspid regurgitation
may mimic that of a VSD. To
distinguish the two the following
clinical signs are useful
TR
Large v waves (also known as cv
waves) on the JVP
Murmur increases in intensity during
inspiration
Pulsatile liver
What are the causes of a VSD?
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The commonest cause is a congenital VSD usually located in the membranous part of the
interventricular septum
But in adults VSD’s are known to occur as a complication of myocardial infarction
What are the complications of a VSD?
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Cardiac failure
Pulmonary hypertension
Reversal of the shunt and Eisenmenger syndrome
Infective endocarditis
Associated valvular lesions – aortic regurgitation
What are the investigations you would like to perform in this patient?
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ECG
The ECG is normal in small VSD’s
In patients with a large VSD there is evidence of left atrial and ventricular enlargement
In patients with pulmonary hypertension there is evidence of right atrial and ventricular
enlargement
CXR
The CXR is normal in patients with a small VSD
In patients with a large VSD there is left ventricular enlargement and pulmonary plethora
If there is associated pulmonary hypertension there is enlargement of the proximal pulmonary
arteries with narrow peripheral vessels and pulmonary oligaemia
Echocardiogram confirms the diagnosis and assesses the severity of the lesion
How would you manage this patient?
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Surgical closure of the lesion is the treatment of choice. The following are indications for surgery
VSD with associated pulmonary hypertension
VSD with symptoms and signs of heart failure
Associated valvular regurgitation
Atrial septal defect
What is the diagnosis?
What are the anatomical types of ASD?
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Ostium primum defect
Ostium secondum defect
What are the complications associated
with an ASD?
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Atrial arrhythmias
Pulmonary hypertension
Reversal of the shunt and Eisenmenger
syndrome
What are the investigations you would like
to perform in this patient?
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ECG
Usually shows right axis deviation and an incomplete RBBB
CXR
Shows pulmonary plethora
Echocardiography
This is used for confirmation of the lesion and anatomy. It also quantifies the severity of the
lesion
How would you manage this patient?
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Surgical closure may be considered in symptomatic patients and those with evidence of
pulmonary hypertension
Cyanotic heart disease in adults
Possible cases for the exam
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Tetralogy of Fallot
Eisenmenger syndrome
Differentiation between these two lesions
TOF
Cyanosis and clubbing
Ejection systolic murmur at the mid left sternal
edge
Soft and single second sound
Eisenmenger syndrome
Cyanosis and clubbing (differential clubbing in
Eisenmenger syndrome due to reversal of a PDA)
Features of tricuspid regurgitation and pulmonary
regurgitation
Loud and palpable P2
Tetralogy of Fallot
What is the diagnosis?
What are the components of the
lesion in TOF?
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Pulmonary infundibular stenosis
Right ventricular hypertrophy
Ventricular septal defect
Overriding aorta
What are the complications associated
with TOF?
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Hypercyanotic spells
Infective endocarditis
Cerebral abscess
Strokes – secondary to polycythaemia
What are the investigations you would like to perform in this patient?
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ECG – shows evidence of right ventricular hypertrophy
CXR – shows a boot shaped heart and pulmonary oligaemia
Echocardiogram is the investigation of choice for confirmation of the diagnosis
Cardiac catheterization is usually performed in order to identify the anatomy before surgical
correction of the lesion
What are the options for management?
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Total correction is the preferred treatment option
However if the patient is not fit for total correction or
has hypoplastic pulmonary arteries a Blalock –Taussig
shunt procedure may be performed as a palliative
procedure
Eisenmenger syndrome
What is the diagnosis?
What are the investigations you would like to perform in this patient?
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ECG – shows right ventricular hypertrophy
CXR – shows dilation of the pulmonary artery with narrowing of the peripheral vessels and right
ventricular enlargement
Echocardiogram
What are the options for management of this patient?
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Monitoring and follow up
Avoid pregnancy
Pulmonary vasodilators
Abnormalities of the arterial pulse
Abnormalities of the arterial pulse may be classified into abnormalities of rate, rhythm and character.
The following details are important and may be asked at any point during a case. Rarely examination of
the pulse may be the only part of your CVS short case
Rate
Abnormality
Tachycardia
Causes
Sinus tachycardia
Arrythmias
Atrial fibrillation
Atrila flutter
SVT
Ventricular tachycardia
Bradycardia
Sinus bradycardia
Arrythmias
Sick sinus syndrome
Second degree heart block
Complete heart block
Rhythm
Irregular pulse
Character
Slow rising pulse
Sinus arrhythmia
Atrial or ventricular ectopics
Atrial fibrillation
Atrial flutter with variable block
Aortic stenosis
Collapsing pulse
Aortic regurgitation
Patent ductus arteriosus
A-V fistula
Causes of a hyperdynamic
circulation
Pulsus alternans
(Alternating small and large
beats)
Severe left ventricular failure
Bisfriens pulse
Mixed aortic valve disease
Pulsus paradoxus
(Excessive fall of pulse pressure
during inspiration)
Cardiac tamponade
Constrictive pericarditis
Discussion
Attach tachycardia and bradycardia management algorithms ALS here
Abnormalities of the JVP
Note
Interpretation of the JVP is extremely difficult at undergraduate level but the following points may be
asked during a discussion
Abnormality
Non pulsatile raised JVP
Loss of “a” wave
Prominent “a” wave
Cannon “a” wave
“cv” waves
Steep “x” and “y” descent
Causes
SVC obstruction
Atrial fibrillation
Tricuspid stenosis
Pulmonary hypertension
Complete heart block
Tricuspid regurgitation
Constrictive pericarditis
Respiratory system
Examination routine
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Introduce yourself and take consent
Ensure adequate exposure and request for a chaperone
if necessary
Proper positioning of the patient at 45 degrees and
make sure that the patient is comfortable
Examination of the respiratory
system
Introduction and consent
Foot end of the bed – Inspection
and general impression
Inspection
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Go to the foot end of the bed
Look around for any clues
Get a general impression of the patient. Is he/she
wasted? Are there signs of respiratory distress?
Look at the chest for any asymmetry, abnormal shape,
deformities and surgical scars
Look for any apical flattening – apical fibrosis
Observe the chest movements
Count the respiratory rate
General examination
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General examination
Sit up patient – Examine trachea
and cervical lymph nodes
Examine from the back
Palpation – Chest movement,
vocal fremitus
Do a general examination relevant to the respiratory
system
Percussion
Face
Febrile/not
Look for central cyanosis, pallor, evidence of Horner’s
Auscultation
syndrome
Neck
Look at the neck veins, assess JVP, look for cervical lymphadenopathy
Examineassess
from the position
front of the
trachea and the distance between the cricoid and the suprasternal notch (These last 3 steps
require the patient to sit up and may be done at a later stage- see examination outline)
Upper limbs
Look for clubbing, cyanosis and nicotine stains in the fingers. Examine the pulse for a bounding
pulse – carbon dioxide retention
Look for flapping tremors – respiratory failure
Look for a mantoux scar
Lower limbs
Look for lower limb edema – cor pulmonale
Respiratory system proper
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Move on to the examination of the respiratory system proper. Ask to start the examination
from the back of the chest as this will reveal the most physical signs
Palpation
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Examine the location of the apex
Feel for a palpable P2 which indicates pulmonary hypertension
Examine the chest movements and look for any asymmetry
Examine the tactile vocal fremitus
Remember to examine all zones of the lung
Percussion
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Percuss in all zones of the lung
Percuss over the liver to look for a pushed down liver dullness
Auscultation
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Auscultate the 3 zones of the lung and listen to the breath sounds. Is there vesicular breathing
or bronchial breathing? Are there any added sounds?
Examine the vocal resonance
Remember to examine all zones of the lung
Interpretation of individual signs in the respiratory system
General examination
Sign
Clubbing
Causes
Infective
Empyema
Lung abscess
Bronchiectasis
Neoplastic
Bronchial carcinoma
Other
Fibrosing alveolitis
Trachea
Deviation towards the lesion
Deviation away from the lesion
Auscultation
Breath sounds
Quality
Bronchial breathing
Intensity
Low intensity
Added sounds
Crepts
Early inspiratory
Consolidation
Localized area of fibrosis
Upper limit of a pleural effusion
Pleural effusion
Consolidation
Pneumothorax
Collapse
Fibrosis
Pneumonia, bronchiectasis
Late inspiratory
Fibrosing alveolitis, pulmonary
edema
Ronchi
Asthma, COPD
Pleural effusion
What are the possible causes you would like to consider?
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Pleural effusions can be categorized into transudative effusions and exudative effusions.
Exudative effusions are commonly unilateral while transudative effusions are commonly
bilateral
Transudative effusion
Nephrotic syndrome
Cardiac failure
Hepatic failure
Hypothyroidism
Exudative effusion
Infective
Parapneumonic effusion
Empyema
Tuberculosis
Malignant
Bronchial carcinoma
Secondary deposits in the pleura
Lymphoma
Mesothelioma
Connective tissue disorders
Rheumatoid arthritis
SLE
Rare
Pulmonary embolism
Pulmonary infarction
Subphrenic abscess
What are the investigations you would like to
perform in this patient?
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Investigations should be performed in this patients
with the following objectives in mind
Confirmation of the diagnosis
Assessment of the severity
Determination of the composition
Determination of the underlying cause
Chest X ray PA and lateral
Pleural aspiration
Send for – full report, cytology, glucose, gram stain and culture, other special investigations
(AFB, LDH, adenosine deaminase)
Investigation
Full report
Interpretation
Neutrophills are raised in acute pleural
inflammation – parapneumonic effusion
Lymphocytes may be raised in malignancy and TB
Glucose content is reduced in parapneumonic
effusion, empyema, TB and malignancy
Important in differentiating between exudative
and transudative effusions
Glucose
Protein
How would you differentiate between an exudative and a transudative
effusion?
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The protein content in an exudative pleural fluid is >3g/l
However for a more accurate diagnosis Light’s criteria is used
Pleural fluid protein: serum protein > 0.5
Pleural fluid LDH: serum LDH > 0.6
Pleural fluid LDH more than 2/3 of the upper limit of normal serum LDH
If 2 or more of the above criteria are met the effusion is classified as exudative
Discuss the principles of management of a pleural effusion
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The basic principles of management are based on the underlying cause of the effusion. The
following table gives a guide to the management
Diagnosis
Management
Parapneumonic
History of
pneumonia
Simple aspiration
Empyema
Is an infection of
the pleural space
TB
History suggestive
of TB
Malignant
Systemic features
Is characterized by
pH <7.2
LDH > 1000
Neutrophills
Aspiration to
dryness
With adequate
antibiotic cover
Demonstration of
organism in
pleural fluid
ADA
Treatment
regimen similar to
that of pulmonary
TB
Malignant cells in
cytology
Observe if
asymptomatic
Therapeutic
aspiration
Pleurodesis
Consolidation
What are the causes you would like to consider in this
case?
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The causes for consolidation of the lung are
Bacterial pneumonia
Bronchial carcinoma
Pulmonary infarction
The most likely cause is bacterial pneumonia
What are the investigations you would like to perform
in this patient?
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CXR for confirmation of the diagnosis
As the most likely cause for consolidation is pneumonia the
further investigations would target this
FBC – to look for neutrophil leucocytosis
Blood culture and ABST
Sputum culture and ABST
What are the principles of management of suspected
bacterial pneumonia?
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Assess the severity
This is usually done by the CURB 65 criteria
Confusion
Urea > 7mmol/l
Respiratory rate > 30 breaths per minute
Blood pressure (Systolic <90 or diastolic <60)
Age > 65
A patient who scores 2 or more of the above criteria should be hospitalized
Obtain the required samples for cultures and commence empirical antimicrobial therapy. These
are usually given intravenously but can be switched to oral antibiotics once the patient is
clinically better
Monitor the vital parameters of the patient and also the response to the antibiotics
The patient should begin to respond within 48-72 hours of initiation of therapy
Continue antibiotics for 5-7 days
CXR may be repeated after about 7-12 days
What will you do if the patient fails to respond to the treatment?
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Reconsider the diagnosis
Reconsider the choice and/ or dose of antibiotics
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Investigate for rare organisms causing pneumonia
Think of the probability of a malignancy
Pneumothorax
What are the causes you would like to consider
in this patient?
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The causes of pneumothorax can be classified as
follows
Spontaneous
Primary – Seen in patients who do not have a
previous history of lung disease. Commonly in tall
thin individuals
Secondary – In patients with lung disease, COPD,
bronchial asthma
Traumatic
How would you manage this patient?
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Assess the severity of the condition
Immediate aspiration may be indicated without radiographic confirmation in a patient with a
tension pneumothorax – severe dyspnoea, marked mediastinal shift, hypotension and
bradycardia
Confirm the diagnosis with CXR PA and lateral
Primary pneumothorax
Aspiration is recommended if the patient is breathless and/or there is a rim of air >2cm on the
chest radiograph
IC tube insertion may be considered if recurrent aspiration is unsuccessful
Secondary pneumothorax
Is considered to have a worse prognosis. Therefore the management plan is different
IC tube insertion is recommended if the patient is breathless + >50 years + rim of air >2cm on
CXR
If the above criteria are not met simple aspiration may be attempted
Lung fibrosis
What are the causes you would consider for pulmonary fibrosis?
The causes of lung fibrosis can be classified as follows
Upper lobe fibrosis
TB
Ankylosing spondylitis
Sarcoidosis
Silicosis
Radiation
Drugs
Lower lobe fibrosis
Rheumatoid arthritis
Scleroderma
Asbestosis
Pneumoconiosis
Paraquat poisoning
Diffuse parenchymal lung
disease
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Are a heterogeneous group of
conditions which share similar
symptoms pulmonary signs,
pulmonary function abnormalities
and radiological changes
Clinical
Exertional dyspnoea, cough with
minimal sputum production
Clubbing
Fine, end inspiratory bi basal
crepitations
CXR
Reticulonodular shadowing
With advanced disease
“honeycombing” of the lung
Pulmonary function testing
Restrictive pattern with reduced diffusing capacity of CO
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Classification
Category
DPLD of known cause or associations
Further classification and causes
Connective tissue diseases
SLE, rheumatoid arthritis, scleroderma
Drugs
Amiodarone
Chemotherapeutic agents
Idiopathic interstitial pneumonias
Granulomatous DPLD
Other rare forms of DPLD
Antirheumatic agents – gold, penicillamine
Environmental exposures
Idiopathic pulmonary fibrosis (formerly known as
fibrosing alveolitis)
Other
Sarcoidosis
Histiocytosis X
What are the investigations you would like to perform in this patient?
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The following investigations are used in the investigative process of a suspected DPLD
Imaging
CXR
HRCT
Pulmonary function tests
Bronchoscopy – Bronchoalveolar lavage
Consider lung biopsy
COPD
What are the principles of management of this patient?
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Given below is a diagram depicting the management of COPD.
Bronchiectasis
What are the causes you would like to consider in this patient?
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Congenital
Cystic fibrosis
Ciliary dysfunction syndromes
Primary hypogammaglobulinaemia
Acquired
Pneumonia (complicating pertussis or measles)
Tuberculosis
Bronchial carcinoma
What are the investigations you would like to perform in this patient?
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CXR
Ring shadows and tramline shadows
HRCT
Sputum culture
What are the principles of management of this patient?
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Chest physiotherapy and postural drainage
Antibiotics
Bronchodilators
Surgical options
Abdominal examination
Examination routine
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Introduce yourself and take consent
Ensure adequate exposure and request for a chaperone if necessary
Position the patient adequately on the bed with one pillow for the head and the arms
comfortably resting at the sides
General examination relevant to the abdomen
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Face
Look for pallor, Icterus, xanthelasmata
Perioral pigmentation
Oral ulcers
Angular stomatitis
Glossitis
Chest
Gynaecomastia
Spider naevi
Upper limbs
Hands
Clubbing, leukonychia, koilonychia
Palmar Erythema
Dupuytren’s contracture
Flapping tremors
Arms
A-V fistulae
Axillary hair
Lymph nodes
Examine both cervical and axillary nodes
Lower limbs
Ankle edema
Skin
Rashes
Inspection of the abdomen



Go to the foot end of the bed and start your inspection from there
Look for the following
Distension
Symmetry of movement of the abdomen
Now come closer and look for the following details
Surgical scars
Dilated veins
Visible pulsations
State of the umbilicus
Any obvious masses or visible peristalsis
Hernial orfices
Palpation



Start the palpation of the abdomen with a superficial palpation moving from quadrant to
quadrant. Always keep your eye on the patient’s face for tenderness
Palpate for the major organs in the abdomen
Liver
Percuss for the upper and lower borders
Spleen
Kidneys
Ask for permission to examine the groin and external genitalia
Percussion



Remember to complete the percussion of any abdominal mass detected then and there
At this stage percuss for free fluid. Initially look for flank and shifting dullness and then go on to
look for horseshoe shaped dullness
If you suspect gross ascites, look for the fluid thrill
Auscultation




Examine for a bruit over the enlarged liver
Examine for a splenic rub
Examine for a renal bruit
Examine the bowel sounds
General points on the presentation and discussion


The usual cases which will be given for the exam usually involve palpable organs. Therefore one
should know how to present a liver, spleen and renal mass
See the table below for the method of presentation
Liver
Right hypochondrial mass
Cannot get above
Moves with respiration
Dull to percussion over the mass
and continues with the liver
dullness
Spleen
Left hypochondrial mass
Cannot get above
Moves diagonally with
respiration
Notch felt/not
Dull to percussion over the mass
and the dullness is continuous
with the splenic dullness
Mention the distance from the
costal margin to the lower
border of the liver in the mid
clavicular line
Mention the distance from the
costal margin to the tip of the
spleen
Renal mass
Mass in the loin
Can get above (If the mass is
very large you may not be able
to get above it)
Moves with respiration
Ballottable
Dull to percussion over the mass
but with the presence of
resonant bands
Measure the size of the lump
from upper to lower pole
Mention the site of the upper
border of the liver (mid clavicular
line
State the span of the liver
Describe the lower border of the
liver, the surface and the
consistency
Describe the consistency of the
spleen
Mention if there is a hepatic
bruit/not
Mention if there is a splenic
rub/not


Describe the consistency
The next step is to know the differential diagnosis for hepatomegaly, splenomegaly,
hepatosplenomegaly and renal mass
Study the following table for the differential diagnosis
Narrowing down your differential diagnosis
Jaundice
Clinical findings
Pre hepatic
Look for pallor
Causes
Hemolytic anaemia
Hepatic
Look for signs of
chronic liver disease
Chronic liver disease
Viral hepatitis
Drug induced hepatitis
Metabolic
Cholestatic
Scratch marks
Cachexia
Intrahepatic
cholestasis
Billiary cirrhosis
Sclerosing cholangitis
Drug induced
Extrahepatic
Pancreatic carcinoma
Gallstones
Hepatomegaly
Clinical picture
Febrile patient +/- jaundice
Peripheral stigmata of chronic liver disease
Hard nodular liver +/- peripheral stigmata of
chronic liver disease
(There may be a hepatic bruit)
Pulsatile liver
Diagnosis
Infective hepatitis
Cirrhosis
Hepatocellular carcinoma
Heart failure, tricuspid regurgitation
Splenomegaly
Based on the size of the spleen
Massive splenomegaly
>8cm or crossing the midline
CML
Myelofibrosis
Chronic malaria
Visceral leishmaniasis
Clinical picture
Moderate splenomegaly
4-8cm
Myeloproliferative disorders
Lymphoma
CLL
Cirrhosis with portal
hypertension
Hemolytic anaemia (Thalassemia)
Diagnosis
Mild splenomegaly
Just palpable or 2-4cm
Myeloproliferative disorders
Lymphoma
CLL
Cirrhosis with portal
hypertension
Infections
Glandular fever
IE
Typhoid
Hemolytic anaemia
Pallor
Lymphadenopathy +/- Pallor
Hemolytic anaemia
Leukaemia, lymphoma
Hepatosplenomegaly
Clinical picture
Pallor
Lymphadenopathy
Peripheral stigmata of liver disease
Diagnosis
Hemolytic anaemia
Myeloproliferative disease
Leukaemia, lymphoma
Leukaemia, lymphoma
Cirrhosis with portal hypertension
Possible discussion topics from a case of hepatomegaly,
splenomegaly or hepatosplenomegaly
Cirrhosis
Hepatocellular carcinoma
Infective diseases of the liver
Hemolytic anaemias
Hematological malignancy
Cirrhosis

Is a pathological term used for progressive diffuse fibrosis of the liver with distortion of the
hepatic architecture and formation of regenerative nodules
What are the possible causes you
would like to consider in this
patient?




Alcohol
Non alcoholic fatty liver disease
Infective
Chronic viral hepatitis
Immune


Autoimmune hepatitis
Bililary
Primary billiary cirrhosis
Secondary billiary cirrhosis
Sclerosing cholangitis
Genetic
Wilson’s disease
Hereditary hemochromatosis
Alpha 1 antitrypsin deficiency
What are the complications of cirrhosis of the liver?






Portal hypertension leading to variceal hemorrhage
Ascites and spontaneous bacterial peritonitis
Hepatic encephalopathy
Hepatorenal syndrome
Coagulopathy
Hepatocellular carcinoma
How would you clinically assess the severity of cirrhosis in this patient?

Severity is assessed by the presence of features of decompensation. These are as follows
Jaundice
Hepatic encephalopathy
Ascites
Bleeding
Portal hypertension
What are the investigations you would like to perform in this patient?





Investigations should be performed to confirm the diagnosis, look for an underlying cause and
to assess the severity and prognosis
FBC
To look for pancytopenia – this could indicate hypersplenism
Liver function tests – these are used to assess severity and prognosis
Serum bilirubin
AST/ALT
PT/INR
Serum albumin
Ultrasound scan of the abdomen
This is used to visualize the liver, look for splenomegaly and ascites
Investigations to look for a cause
Remember that alcoholic liver disease is the most common cause, but other causes may be
considered if the history is not suggestive
Hepatitis B serology
Serum autoantibodies
Serum iron and ferretin – Haemochromatosis
Serum ceruloplasmin – Wilson’s disease
Liver biopsy
What are the principles of management?



Treat the underlying cause if possible
Manage complications
Ascites
Hepatic encephalopathy
Variceal bleeding
(See long cases in medicine for a further discussion on these topics)
Liver transplantation
This is based on a scoring system – i.e. Child-Pugh classification or MELD scoring system
Hepatocellular carcinoma
What are the causes you would consider in this patient?

Remember that most of the time hepatocellular carcinoma occurs in a cirrhotic liver. Therefore
all causes for cirrhosis may be considered
What are the investigations you would
like to perform in this patient?



Ultrasound scan of the abdomen
This will detect any focal lesions in the
liver
Serum markers
Alpha fetoprotein
Remember that liver biopsy is not
indicated as seeding of the tumor can
occur along the biopsy tract
What are the options for management in this patient?

The therapeutic options for management are
Resection
Liver transplant – preferred in patient with cirrhotic livers
Percutaneous ablation
TACE (Transarterial chemo-embolization)
Chemotherapy
Viral hepatitis





Is caused mainly by hepatitis viruses A-E but can also
be caused by other viruses such as CMV and EBV
The clinical course is usually described in 4 phases.
These are the incubation, prodrome, icteric phase
and recovery phase
Investigations in the initial phase
FBC – Decreased WCC with a relative lymphocytosis
Liver function tests – Elevated AST with normal
serum bilirubin
Specific investigations
Include those for the diagnosis (See table below)
Management is usually supportive
Hepatitis A
Hepatitis B
Microbiology
Complications
Investigations
RNA virus
Transmission is via
the faeco-oral
route
Acute fulminant
hepatitis
Prodrome
HAV in stool (by
electron
microscopy or
RNA detection.
This is not
commonly used
DNA virus
Transmission is by
the intravenous
route, sexual
contact
Vertical
transmission can
also occur
Chronic infection
Asymptomatic
carrier
Cirrhosis
Hepatocellular
carcinoma
Acute fulminant
IgM HAV
Positive at the
onset of
symptoms.
Persists for about
4-6 months
HBsAg and
positive IgM antiHBc
Indicates acute
hep B infection
HBeAg
Indicates severe
Management and
Prevention
Personal hygiene
Vaccination
Vaccination
hepatitis is rare
infection
HBsAg persisting
for more than
6months with
positive IgG antiHBc and negative
IgM anti-HBc
Indicates chronic
infection
Hepatitis C
RNA virus
Transmission is via
the intravenous
route and by
sexual contact
Hepatitis D
Incomplete RNA
particle
Can only replicate
in the presence of
hepatitis B
infection
This can be
superinfection
(infection in a
person already
having hep B) or
coinfection
RNA virus
Similar to Hep A
Hepatitis E
Higher risk of
developing chronic
liver disease,
cirrhosis and
hepatocellular
carcinoma
Acute fulminant
hepatitis more
common in
coinfection
Chronic liver
disease more
common in
superinfection
Fulminant
hepatitis
Anti HCV
Vaccine?
Co infection
IgM anti HDV and
IgM anti HBc
Vaccine?
Superinfection
IgM anti HDV and
IgG anti HBc
HEV RNA in stools
No effective
prophylaxis
Hemolytic anaemia


Basic investigation of a suspected hemolytic anaemia starts with the FBC and blood picture. The
blood picture has a specific appearance according to the type of hemolytic anaemia
Other investigations
Reticulocyte count - Increased reticulocytes


Unconjugated hyperbilirubinaemia
Hemoglobinuria and hemosiderinuria in intravascular hemolysis
Bone marrow – erythroid hyperplasia
After confirmation of a hemolytic anaemia investigations should focus on finding the cause or
underlying pathology
Classification of hemolytic anaemia is into congenital and acquired
Congenital
Membrane defects
Hereditary spherocytosis
Hereditary elliptocytosis
Metabolic defects
G6PD deficiency
PK deficiency
Disorders of hemoglobin
Thalassemia
Sickle cell anaemia
Acquired
Immune
Autoimmune
Warm
Cold
Alloimmune
Transfusion reactions
Hemolytic disease of the newborn
Red cell fragmentation syndromes
Prosthetic valves
HUS, TTP, DIC
Systemic disease
Infection
Toxins
Congenital hemolytic anaemias
Disease
Hereditary spherocytosis
(AD)
Investigations
Blood film – Spherocytes
Osmotic fragility test
G6PD deficiency
(X linked)
Hb normal between attacks
Blood film – Bite cells, blister
cells, Heinz bodies
Features of intravascular
hemolysis
G6PD levels in the RBC
Thalassemia
β – Thalassemia major
Blood film - microcytic
hypochromic anaemia
Target cells, nucleated red blood
cells
Reticulocyte count may be low
Serum iron studies
Management
Definitive management is
splenectomy which is usually
planned when the child is 5-6
years of age
In the meantime the
management is based on
symptoms with severe anaemia
managed by blood transfusion
Is precipitated by antioxidant
drugs and substances
Avoiding these is the most
important aspect of the
management
A crisis can be treated with blood
transfusions as necessary
Management is with recurrent
blood transfusions
Consider splenectomy
Monitor for the complications of
iron overload
Cardiomyopathy
Bone marrow – Erythroid
hyperplasia
Serum hemoglobin
electrophoresis- Absent HbA
with increased HbF and HbA2
Sickle cell anaemia
Blood film - Sickle cells, HowellJolly bodies
Sickling test
Hb electrophoresis - HbS
Liver disease
Endocrine organ dysfunction –
growth, hypothyroidism, diabetes
Iron chelation therapy
Subcutaneous desferrioxamine
Can cause auditory and
ophthalmological side effect
Counseling and parent education
Rare in SL
Avoid precipitants
Management of crisis with
analgesia, adequate fluid and
transfusion
Acquired hemolytic anaemia
Type of antibody
Causes
Investigations
Management
Warm AIHA
IgG
Idiopathic
Autoimmune – SLE
Lymphoma
CLL
Drugs – Methyldopa
Those of hemolytic anaemia
Spherocytes on the blood film
Treat cause
Blood transfusion of necessary
Steroids
Immunosuppressive drugs –
Azathioprine, cyclophosphamide
IVIg
Splenectomy is also a final
option of there is poor response
to the medical management
Cold AIHA
IgM
Idiopathic
Infections – EBV, CMV
Mycoplasma
Those of hemolytic anaemia
Less spherocytes
Cold agglutination test
Treat cause
Keep warm
Hematological malignancy
Leukaemias


Classified as acute and chronic leukaemias
In acute leukaemia there is proliferation of primitive stem cells causing accumulation of blasts in
the bone marrow


In chronic leukaemia the malignant cells retain the ability to differentiate causing accumulation
of cell of various levels of differentiation
Acute leukaemia occurs at all ages. ALL has a peak incidence at 1-5 years
Chronic leukaemia occurs in middle and old age individuals
Acute leukaemia
Clinical presentation
Associations
Investigations
Management
ALL
Features of bone marrow failure
Organ infiltration
Trisomy 21
Translocation (9:22)
FBC – Pancytopenia
Blood picture – Blasts
Bone marrow - >30% blast cells
Special stains and classification
tests
General supportive therapy
Chemotherapy
Induction of remission
Prednisilone
Consolidation of remission
Intensive multi agent
chemotherapy
CNS prophylaxis
Intensification
Maintenance chemotherapy
AML
Features of bone marrow failure
Organ infiltration
Can have other features
DIC, gum hypertrophy
Similar
Positive for myeloperoxidase
stain
General supportive therapy
Induction of remission
Consolidation
Chronic leukaemia
Clinical presentation
CML
Presents usually with insidious
features
Can also present mimicking an
acute leukaemia. This is known
as a blast crisis
CLL
Presents with insidious features
Associations
Investigations
Management
Philadelphia chromosome (95%)
FBC
High leucocyte count
Normocytic normochromic
anaemia
Thrombocytosis
Blood picture
Full range of granulocyte
precursors and mature
neutrophils
This varies on the stage of the
disease
Chronic stage
Tyrosine kinase inhibitors Imatinib
Accelerated and blast phase
Tyrosine kinase inhibitors if the
patient has not already been
given one
Hydroxycarbamide
FBC
Lymphocytosis
Associated autoimmune
hemolytic anaemia
Blood picture
Lymphocyte precursors and
mature lymphocytes
Has a better prognosis.
Treatment is only required if the
patient is progressively
symptomatic or if there is
evidence of marrow failure
Chlorambucil
Lymphomas
Hodgkin’s lymphoma
Clinical
Investigations
Management
Non Hodgkin’s lymphoma
Lymphadenopathy usually begins Has a more unpredictable and
from 1 group of peripheral
haphazard spread
lymph nodes and spreads
contiguously to the others
Can have mediastinal
involvement
Involves oropharyngeal lymph
nodes
Extra nodal spread rare
Leukaemic phase rare
Extra nodal spread common
Leukaemic phase more common
Constitutional symptoms
common
Lymph node biopsy shows Reed
– Sternberg cells
Early stage disease
Radiotherapy
Constitutional symptoms rare
Advanced disease
Chemotherapy +/- radiotherapy
No RS cells
Multi agent chemotherapy
Polycystic kidney disease
What are the main genetic categories of PCKD?


Autosomal dominant PCKD – presents with renal failure in adults
Autosomal recessive PCKD – presents with renal failure in
childhood
What are the complications known to be associated
with PCKD?


Renal complications
Renal failure
Hypertension
Cyst rupture
Cyst infection
Renal calculi
Urinary tract infection
Extra renal complications
May be associated with cysts in other sites – liver, ovary, pancreas
Berry aneurysms
Ascites
What are the causes you would like to consider in this
patient?



There are 2 clinical patterns of ascites encountered in clinical
practice. These are
Ascites out of proportion to ankle edema
Portal hypertension
Intra abdominal malignancy
Tuberculous peritonitis
Constrictive pericarditis
Ascites as a part of generalized edema
Heart failure
Nephrotic syndrome
How would you clinically evaluate this patient for a cause?
Clinical pattern
Ascites out of proportion to
ankle edema
Cause
Portal hypertension
Intra abdominal malignancy
Constrictive pericarditis
Ascites as a part of generalized
edema
Heart failure
Nephrotic syndrome
Further examination
Stigmata of chronic liver disease,
splenomegaly
Ovarian carcinoma is a
recognized cause. Therefore
suspect this in cachetic females
Steep x and y descent in the JVP
Pulsus paradoxus
Pericardial knock
Elevated JVP
Hepatomegaly
Ask to examine the urine for
protein
What are the investigations you would like to perform in this patient?




Ultrasound scan of the abdomen – to visualize the intra abdominal organs
UFR
Tumor markers – CA 125 in females
Diagnostic peritoneal tap – full report, cytology
How would you determine whether the ascitic fluid is exudative or
transudative?



This is based on the serum albumin – ascitic fluid gradient (SAAG)
If the SAAG is <1.1g/dl it is exudative
If it is more than 1.1g/dl it is transudative
What are the principles of management?


Treat the underlying cause
Symptomatic treatment of ascites
Dietary management with salt restriction
Diuretics – spiranolactone and frusemide
Therapeutic paracentesis
Nervous system
Examination routine
Examination of the cranial nerves



Introduce yourself and take consent
Ask for a chaperone if required
Look for any obvious abnormalities – ptosis, squint, facial asymmetry
Cranial nerve 1

Routinely not tested but the patient can be asked on his/her sensation of smell
Cranial nerve 2




Start with examination of the visual acuity using a pocket Snellen chart. If the patient cannot see
this go on to the finger counting method
Examine the visual fields using the confrontation method. The technique of examination is
extremely important
Examine the pupils – size, shape, symmetry, direct and consensual light reflex and
accommodation reflex
Ask the examiner for the ophthalmoscope to examine the fundi
Cranial nerves 3, 4 and 6



Look for ptosis
Examine the eye movements in all directions
Note any nystagmus
Cranial nerve 5







Motor
Test the masseters by asking the patient to clench his/her teeth. Feel the muscle bulk of the
contracting muscle
Test the pterygoids by asking the patient to open his/her mouth. Look for any deviation. Test
again after applying resistance
Test the jaw jerk
Sensory
Examine the facial sensation
Examine the corneal reflex
Cranial nerve 7

Test the muscles of facial expression in the upper and lower half of the face respectively

Taste is not tested routinely
Cranial nerve 8



This is also not routinely examined at the short cases
Whispering test
Rinne’s and Weber’s test
Cranial nerve 9 and 10


Ask the patient to open his/her mouth. Observe the symmetry of the palate
Ask the patient to say “aah” and look for any deviation of the palate or a lack of movement
Cranial nerve 11

Examine the trapezius and sternocleidomastoid muscles
Cranial nerve 12



Inspect the tongue in the resting position within the mouth. Look for wasting and fasiculations
Ask the patient to protrude the tongue and look for any deviation
Check the power of the tongue
Remember that in the exam usually the command is to examine only the motor component of the
cranial nerves
Lesions of the visual pathway
Where is the lesion?
What is the pathology?


The most important lesion of the above pathway is that at the optic chiasm. Abnormalities of
the pituitary gland is responsible most of the time
Given below are the causes
Pituitary tumor – Look for features of acromegaly
Craniopharyngioma
Suprasellar meningioma
Gliomas
Vascular lesions – aneurysms
Ptosis
Where is the lesion?
Ocular myopathy
(Muscle)
Bilateral and
symmetrical
Myasthenia gravis
(NMJ)
Initially one side is more
affected than the other
Pupils are not involved
3rd nerve palsy
(Nerve)
Ptosis
Affected eye deviated
laterally and
downwards
Fatigability
Pupil may or may not
be dilated
Horner’s syndrome
(Sympathetic)
Partial ptosis
Constricted pupil
Enophthalmos
Anhydrosis
3rd nerve palsy
Where is the lesion?



The classification of 3rd nerve palsy is as follows
Surgical 3rd nerve palsy – Here the pupillomotor fibers of the
3rd nerve are affected causing dilation of the pupil
Seen in lesions of the midbrain and compression of the 3rd
nerve along its course
Medical 3rd nerve palsy – Here the pupil is unaffected
Surgical 3rd nerve palsy

The lesion can be localized based on the pathway of the 3rd
cranial nerve
Midbrain
Lies in close relationship
with the corticospinal
tracts and the red
nucleus
Exit from the midbrain
Lies in close relationship
with the posterior
communicating artery
Cavernous sinus
Lies in close relationship
with the 4th and 6th
cranial nerves and the
ophthalmic and
maxillary branches of
the 5th CN
Orbit
Lies in close relationship
with the 4th and 6th
cranial nerves and the
ophthalmic branch of
the 5th CN
Lesion
3rd nerve palsy +
contralateral
hemiplegia (Weber
syndrome)
Lesion
Isolated surgical 3rd
nerve palsy
Lesion
Associated 4th and 6th
nerve palsies and
sensory loss of the face
in the ophthalmic and
Lesion
Associated 4th and 6th
nerve palsies and
sensory loss of the face
in the ophthalmic
maxillary divisions
division
rd
3 nerve palsy +red
nucleus - tremor and
involuntary movements
(Benedikt’s syndrome)
What is the pathology?
rd
Surgical 3 nerve
Site
Midbrain
Exit from the midbrain
Medical 3rd nerve
Cavernous sinus
Orbit
Nerve
Pathology
Vascular lesion – infarct
Tumor
Posterior communicating artery
aneurysm
Cavernous sinus thrombosis
Tumor
Hypertension, DM, vasculitis, MS
Myasthenia gravis
What are the investigations you
would like to perform in this patient?




Edrophonium (Tensilon test)
This is an important test to aid in the
diagnosis. Edrophonium is a short acting
acetylcholinesterase inhibitor. This is
injected IV and response is observed
EMG
Repetitive stimulation test will show a
decremental response
Antibody testing
Acetylcholine receptor antibodies (over
80% of cases)
CXR/ CT thorax
To look for evidence of a thymoma
What are the options for management in a patient with myasthenia gravis?





Anticholinesterase drugs
Pyridostigmine
Thymectomy
Corticosteroids
Other immunosuppressant therapy – azathioprine
IV immunoglobulin or plasma exchange in a myasthenic crisis
Horner syndrome
Where is the lesion?
Given below is the localization of the important sites of the lesion in a patient with Horner syndrome
Brainstem
Associated with lateral
medullary syndrome
T1 root
Look for small muscle wasting in
the hands
Examine the lungs to look for
evidence of a tumor in the apex
of the lung (Pancoast’s
syndrome)
Neck
Look for local lymphadenopathy,
masses, aneurysms
6th nerve palsy
Where is the lesion?
What is the pathology?
At the brain stem
(Pons)
The 6th nerve nucleus
lies in close proximity
to the nucleus of the 7th
nerve and the
corticospinal tract
Intracranial course
(nerve)
Has the longest
intracranial course of all
cranial nerves. Lies close
to the tip of the petrous
temporal bone
Cavernous sinus
Orbit
Lies in close relationship
with the 3rd and 4th
cranial nerves and the
ophthalmic and maxillary
branches of the 5th CN
Lesion
6th nerve palsy + LMN
7th nerve palsy +
contralateral
hemiplegia
Lesion
Isolated 6th nerve palsy
Pathology
Infarction of the pons
Tumor
Pathology
Increased intracranial
pressure
Basal meningitis
Inflammation of the
petrous tip
Diabetes
Hypertension
Lesion
Associated 3rd and 4th
nerve palsies and
sensory loss of the face
in the ophthalmic and
maxillary divisions
Pathology
Cavernous sinus
thrombosis
Lies in close
relationship with the
3rd and 4th cranial
nerves and the
ophthalmic branch of
the 5th CN
Lesion
Associated 3rd and
4th nerve palsies and
sensory loss of the
face in the
ophthalmic division
Pathology
Tumor of the orbit
7th nerve palsy
Where is the lesion?
What is the pathology?


The most important step in localizing the site of lesion in a facial
nerve palsy is to determine whether it is a UMN lesion or a LMN
lesion
Both upper and lower parts of the face would be affected in a
LMN lesion while only the lower part of the face would be
affected in an UMN lesion

See the diagram given below
Clinical type
Site of lesion
Associated features
Pathology
UMN
Above the facial nucleus
located in the pons
Usually at the level of the
cortex or internal capsule
Infarction
Tumor
LMN
Pons
Cortical lesions
Associated dysfunction of
speech (dysphasia) and loss
of other higher functions
Hemiplegia
Associated ipsilateral 6th
nerve palsy and
contralateral hemiplegia
th
Cerebellopontine angle
Associated 5 nerve palsy
th
and 8 nerve palsy
Internal acoustic meatus
Associated 8 nerve palsy
Inner ear
Check for hyperacousis and
taste of the anterior 2/3 of
the tongue, look for vesicles
in the external auditory
canal
External acoustic meatus
Parotid gland
Infarction
Tumor
CP angle tumor –
acoustic neuroma
th
th
Isolated 7 nerve palsy
CSOM, cholesteatoma,
Ramsay Hunt
syndrome
Bell’s palsy
Parotid tumors
What are the treatment options available for Bell’s palsy?
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Most patients recover spontaneously
Physiotherapy
Electrical stimulation of the facial nerve
Steroids
Acyclovir
Nystagmus and cerebellar signs
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There are clinical types of nystagmus. These are jerky nystagmus and pendular nystagmus
Pendular nystagmus
Oscillations are equal in speed and amplitude in both directions. Seen in patients with severe
refractory error and macular disease
Jerky nystagmus
Has a fast phase and a slow phase. Seen in patients with cerebellar disease, vestibular disease
and disorders of their central connections
What are the cerebellar signs you would elicit in this patient?
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Scanning dysarthria
Past pointing
Rebound phenomenon
Dysdiadochokinesia
Pendular knee jerk
Heel shin test
What are the causes of cerebellar syndrome?
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Congenital anomalies – Agenesis of the cerebellar vermis, Dandy – Walker malformation
Cerebellar infarction
Demyelination - MS
Cerebellar tumors - Medulloblastoma
Infections
During infections – coxsackie, echo, EBV
Postinfectious – varicella
Degenerative conditions – Friedrich’s ataxia, ataxia telangectasia, Batten’s disease
Drugs and toxins – Phenytoin, alcohol
Paraneoplastic syndromes – bronchial carcinoma
Lesions of the lower cranial nerves
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This involves lesions of the CN 9, 10 and 12
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Try to identify the clinical pattern of the lesion. These are given below
Bulbar palsy and pseudobulbar palsy
How would you differentiate between bulbar palsy and pseudobulbar palsy?
Anatomical basis
Features
Pseudobulbar palsy
Is an upper motor neuron lesion
of the cranial nerves 5, 9, 10, 11
and 12
(The cranial nerves arising from
the medulla)
Emotionally labile
Dysarthria (‘Donald Duck’
speech)
Dysphagia
Spastic tongue
Palatal movements impaired
Exaggerated jaw jerk
Bulbar palsy
Is a lower motor neuron lesion of
the cranial nerves 5, 9, 10, 11
and 12
Not emotionally labile
Dysarthria (nasal speech)
Dysphagia + nasal regurgitation
Tongue wasting and fasciculation
Palatal movements impaired
Normal or absent jaw jerk
What are the causes for bulbar palsy and pseudobulbar palsy?
Pseudobulbar palsy
Stroke
Demyelinating disease
Lateral medullary syndrome
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Is characterized by the following
Ipsilateral Horner syndrome
Ipsilateral 10th nerve palsy
(palate)
Ipsilateral cerebellar signs
Ipsilateral sensory loss of the
face
Contralateral sensory loss of the
body
Bulbar palsy
TB meningitis
MND
Myasthenia gravis
12th nerve palsy
Where is the lesion?
What is the pathology?
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The most important aspect of a 12th nerve palsy is to identify whether the lesion occurs as a part
of bulbar palsy or in isolation
Neurological examination of the lower limbs
Examination routine
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Introduce yourself and obtain consent
Ask for a chaperone if necessary
Ensure adequate exposure of the lower limbs
Start with an examination of the gait
Inspection
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Make sure to inspect the limbs carefully for muscle wasting and fasiculations. Tap the muscles of
the thigh and leg to elicit fasiculations if they are not seen
Look for scars – muscle biopsy scars and tendon release scars
Tone
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Ask the patient to relax
Assess the tone of the lower limbs around all major joints – hip, knee and ankle
Then put your hand behind the patient’s knee and flick it upward – this assess the tone around
all 3 joints at the same time
If the tone is high check for ankle clonus and patellar clonus
Power
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Hip
Knee
Ankle
Given below are the important muscle groups to be examined and their root values
Remember to initially examine the movement without resistance and then with resistance
Muscle action
Flexion
Adduction
Abduction
Extension
Extension
Flexion
Dorsiflexion
Plantarflexion
Inversion
Eversion
Root value
L1, L2
L2, L3
L4, L5
L5, S1
L3, L4
L5, S1
L4, L5
L5, S1
L4, L5
L5, S1
Muscle and nerve
Iliopsoas – Femoral
Adductors – Obturator
Gluteus medius – Superior gluteal
Gluteus maximus – Inferior gluteal
Quadriceps – Femoral
Hamstrings - Sciatic
Tibialis anterior – common per.
Gastrocnemius – tibial nerve
Tibialis posterior – tibial nerve
Peroneal – common per.
Grading of muscle power
Grade
5
4
Description
Normal power
Can move against resistance but sub optimal
power
Can move against gravity but not against
resistance
Cannot move against gravity but can move when
the effect of gravity is eliminated
Flicker of movement
No movement
3
2
1
0
Reflexes
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Examine the following important reflexes. Make sure that the patient is relaxed
Knee – L3, L4
Ankle – L5, S1
Plantar reflex
If the reflexes are not elicited use reinforcement and re check
Coordination
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Perform the heel-shin test to look for coordination
Remember that this test should only be performed if the
muscle power is normal
Sensory
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Usually not examined at the exam
Interpretation of physical signs – LL examination
The two most important questions to be answered in a neurology case are
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Where is the lesion
What is the pathology
The interpretation of physical signs starts with
UMN lesion or a LMN lesion?
Upper motor neuron lesion
Increased tone
Increased reflexes
Ankle and patellar clonus may be present
Extensor plantar response
Lower motor neuron lesion
Decreased tone
Diminished or absent reflexes
Plantars may be flexor or equivocal
Approach to a LMN lesion
If the lesion is a lower motor neuron lesion further analyze your findings to localize the site of the lesion
Site of the lesion
Muscle
NMJ (Not given at the exam)
Peripheral nerve
Root
Anterior horn cell
Spinal cord lesions
Pattern of neurological signs
Bilateral and symmetrical weakness
Proximal>Distal weakness
Reflexes – Knee jerk is lost while the ankle jerk may
be preserved
Waddling gait and Gower sign positive
No sensory impairment
Fatigable weakness
Polyneuropathy
Bilateral and symmetrical weakness
Distal>Proximal weakness
Sensory may or may not be impaired. If impaired will
be in a glove and stocking distribution
Mononeuropathy
Motor and sensory pattern related to the supply of
the nerve
Multifocal neuropathy (Rarely given as cases)
Patchy involvement of peripheral nerves
Will have motor and sensory loss in a root
distribution
Bilateral and symmetrical weakness
Proximal>distal
Prominent wasting and fasiculations
No sensory impairment
Spinal cord lesions may present as LMN lesions
Associated bladder and bowel incontinence
Sensory level
Possible further discussions from a case of LMN of the lower limbs
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Proximal myopathy
Peripheral neuropathy
Foot drop
Proximal myopathy
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There are two important categories of muscle disorders causing proximal myopathy. These are
myopathies and muscular dystrophies
The only important muscular dystrophy at undergraduate level is Becker’s muscular dystrophy
Myopathies can be classified according to their aetiology as given below
Congenital
Inflammatory
Endocrine and metabolic
Toxic
Drugs
Neoplastic
Causes
Metabolic myopathies
Due to disorders in carbohydrate
and lipid metabolism
Dermatomyositis
Polymyositis
Hypo and hyperthyroidism
Cushing’s syndrome
Conn’s syndrome
Hypokalemia
Alcohol
Organophosphates
Corticosteroids
Statins
Paraneoplastic syndromes
Peripheral neuropathy
Polyneuropathy
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The following table lists the possible causes of polyneuropathy
Congenital
Hereditary motor and sensory neuropathy
(HMSN)
Acquired
Infection
Leprosy
Diphtheria
Inflammatory
Guillain- Barre syndrome
CIDP
Vasculitis and connective tissue disease
Metabolic and endocrine
DM
Vitamin deficiency – B1, B6, B12, E
Organ failure
Chronic renal failure
Drugs
Toxins
Arsenic
Lead
Organophosphates
Malignancy
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Investigation of a suspected neuropathy should be started with a nerve conduction study. Then
specific investigations should be performed to find the possible cause
The NCS identifies 2 major categories of peripheral neuropathy
Demyelinating – Reduced nerve conduction velocity
Axonal – Reduction in the amplitude of the action potential with relative preservation of the
conduction velocity
Guillain – Barre syndrome
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Is a post infectious demyelinating disease
Diagnosis is on clinical suspicion. Presents as an ascending paralysis which may follow a
respiratory tract infection or an episode of diarrhea
Management
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The most important aspect of the management is close monitoring of the patient. The following
are the most important
Progression of the neurological symptoms and signs
Respiratory function
This is done with the single breath count and cough effort at the bedside. A more accurate
assessment can be made by a respirometer
Autonomic function
A life threatening complication is autonomic dysregulation. Therefore monitor the pulse rate
and blood pressure
If there is deterioration in the respiratory function ICU care is necessary
IV IG or plasmapharesis is used as the definitive management
The child should be given limb and chest physiotherapy and DVT prophylaxis until recovery
Proper nursing care is essential
Investigations
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Confirmatory investigations
LP – shows cytoprotein dissociation with elevated proteins and normal white cell count
Nerve conduction study
Foot drop
Where is the lesion?
There are 2 types of foot drop encountered in clinical
practice. These are UMN type foot drop and LMN type
foot drop. The latter is usually given as a short case
Cortex and spinal
cord
UMN lesion
L4/L5 root lesion
Sciatic nerve
Common peroneal
Polyneuropathy
Weakness of
inversion
Weakness of all
muscles from the
knee downwards
(Knee extension
spared – femoral)
Weakness of
dorsiflexion and
eversion. No
weakness of
inversion
B/L foot drop
Ankle reflex
preserved
Ankle reflex lost
Ankle reflex lost
Loss of ankle
reflexes B/L
Sensory loss over
the lateral calf and
dorsum of the foot
Stocking type
sensory loss
Sensory loss in the Sensory loss in
L4, L5
sciatic territory
dermatomes
Approach to an UMN lesion
After identification of an upper motor neuron lesion think of the clinical pattern
Clinical pattern
Hemiplegia
Spastic quadriplegia
Possible sites of the lesion
Cortex
Further localization
Look for associated
disturbances of higher
function + UMN facial nerve
palsy
Internal capsule
Usually presents only with
motor manifestations
Brain stem
Examine for cranial nerve
palsies
Look for associated bladder
and bowel incontinence and a
sensory level
Cervical cord
Brain stem
Spastic paraplegia
Spinal cord between T1 and L1
Examine for cranial nerve
palsies
Look for associated bladder
and bowel incontinence and a
sensory level
Examine the superficial
abdominal reflexes for further
localization
Remember –
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When you pick up UMN signs in the lower limbs always examine the upper limbs and do a quick
cranial nerve examination to localize the lesion as given above
Possible discussions from and UMN lesion in the lower limbs
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Hemiplegia
Spastic quadriplegia
Spastic paraplegia
Hemiplegia
Stroke
What are the causes you would like to consider in this patient?
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There are two major categories of stroke. These are ischaemic stroke and hemorrhagic stroke.
Given below are the causes of ischaemic stroke
Pathology
Athero-thromboembolism
Cardioembolism
Arterial dissection
Vasculitis
Hematological
Other
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Causes/ risk factors
DM, smoking, Hyperlipidaemia, hypertension
Atrial fibrillation
Infective endocarditis
Intramural thrombus secondary to an MI
Carotid artery dissection
SLE
Infective vasculitis – HIV, syphillis
Hemoglobinopathy – Sickle cell anaemia
Hyperviscosity syndrome – polycythaemia, MM,
macroglobulinaemia
Hypercoagulable states – Protein c deficiency,
protein s deficiency, factor V Leiden
APLS
Hyperhomocysteinaemia
The aetiology depends on the age of the patient. Atherosclerosis would be the commonest
cause in most patients but the other causes should be excluded in young patients
What are the aspects of management in a patient with a
stroke?
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Stabilize the A,B,C of the patient
Check and stabilize the blood glucose of the patient
Imaging studies should be carried out – CT/ MRI
Look for the possibility of administering thrombolytics (rtPA). Check
inclusion and exclusion criteria
Continue monitoring the vital signs of the patient
Nursing care – bladder, bowel, skin
Nutrition
Rehabilitation
Management of risk factors
What are the investigations you would like to perform in this patient?
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After the acute stage most of the investigations would be focused on finding an aetiology for the
stroke
Lipid profile, FBS
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Echocardiogram
Vasculitic screen
HIV testing, VDRL
Clotting studies
Serum homocysteine
Spastic quadriplegia and spastic paraplegia
Spinal cord disease
What are the causes you would like to consider in this case?
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Spinal cord disease can be classified as compressive and non compressive. The following table
gives the causes
Compressive spinal cord disease
Site
Vertebral
Causes
Trauma
Intervertebral disc prolapse
Metastatic carcinoma
Myeloma
TB
Tumors – meningioma, neurofibroma, lymphoma
Epidural abscess
Tumors – Glioma
Metastasis
Meninges
Spinal cord
Non compressive spinal cord disease
Type
Congenital
Causes
Hereditary spastic paraplegia
Infective/ inflammatory
Vascular
Transverse myelitis
Anterior spinal artery thrombosis
Metabolic
Vitamin B12 deficiency
Degenerative
MND
Syringomyelia
Important features
AD
Onset usually in adult life
Dorsal columns
(Proprioception and
vibration) spared
Loss of propriception, loss of
ankle jerks due to associated
peripheral neuropathy
Mixture of UMN, LMN,
bulbar palsy
Dissociated sensory loss
What are the investigations you would like to perform on this patient?
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X rays of the spine
MRI of the spine
Other investigations to look for a cause
Abnormalities of the gait
Gait
Hemiplegic
Bilateral spastic
Cerebellar
Parkinsonian
Sensory ataxic gait
High stepping
Waddling gait
Description
Circumduction with the
upper limb of the
affected side flexed at
the elbow and pronated
Looks as if the patient is
wading through water
Broad based and
unsteady gait
Short shuffling steps
Lack of arm swing
Stooped posture
Festinant gait
Stamping gait, broad
based, patient looks to
the floor to aid unsure
steps
Foot drop
Further examination
LL examination for
UMN signs, UMN facial
nerve palsy
Possible causes
Stroke
Tumor
UMN signs in the lower
limbs
Look for other
cerebellar signs
Other signs of
Parkinson’s disease –
bradykinesia, rigidity,
asymmetrical resting
tremor
Positive Romberg’s sign
Impaired
proprioception and
vibration sense
Examine LL
Spinal cord disease
Look for possible causes
of proximal myopathy
Alcohol
Cerebellar degeneration
Parkinson’s disease
Subacute combined
degeneration of the
cord
Tabes dorsalis
See discussion on foot
drop
Proximal myopathy
Neurological examination of the upper limbs
Examination routine
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Introduce yourself and take consent
Ask for a chaperone if necessary
Ensure adequate exposure of the upper limbs
Inspection
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Make sure you inspect the upper limbs very carefully for evidence of muscle wasting. Look
especially over the deltoids, inspect the area over the scapula and look at the muscles of the
palmar and dorsal surface of the hand
Look for fasiculations in the major muscle groups of the upper limbs. Tap over the muscle to
elicit fasiculations
Look for surgical scars
Ask the patient to hold out the hands and observe for any abnormal movements
Look for wrist drop
Look for pronator drift
Tone
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Ask the patient to relax
Examine the tone around all important joints of the upper limbs – shoulder, elbow and wrists
Power
Shoulder
Elbow
Wrist
Fingers
Muscle action
Abduction
30 degrees
Further
Adduction
Internal rotation
External rotation
Flexion
Extension
Flexion
Extension
Flexion
Root value
Muscle and nerve
C5, C6
C5. C6
C6, C7
C5, C6
C5, C6
C5, C6
C7, C8
C7, C8
C7, C8
C7, C8
Supraspinatus – Suprascapular
Deltoid - Axillary
Pec major, lat dorsi
Subscapularis – Subscapular
Infraspinatus - Suprascapular
Biceps – Musculocutaneous
Triceps - Radial
Wrist flexors – Ulnar and median
Wrist extensors - Radial
Wrist flexors – Ulnar and median
Extension
Abduction
Adduction
Flexion, extension,
opposition
Thumb
C7, C8
T1
T1
T1
T1
Wrist extensors – Radial
Dorsal interrossei – Ulnar
Palmar interossei – Ulnar
Flexor pollicis, opponens pollicis Median
Grading of muscle power
Grade
5
4
Description
Normal power
Can move against resistance but sub optimal
power
Can move against gravity but not against
resistance
Cannot move against gravity but can move when
the effect of gravity is eliminated
Flicker of movement
No movement
3
2
1
0
Reflexes
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Examine the following important reflexes. Make sure that the patient is relaxed
Biceps – C5, C6
Triceps – C7, C8
Supinator – C6, C7
If the reflexes are not elicited use reinforcement and re
check
Coordination
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Do the finger nose test and examine for
dysdiadokokinesia
In order to examine for coordination the muscle power
should be normal
Sensory
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Examine the dermatomes
Anatomy of the nerves of the upper limb
Wasting of the small muscles of the hand
Where is the lesion?
What is the pathology?
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The 1st step is to determine the pattern of muscle wasting and muscle weakness
There could be 3 possible scenarios
All muscles involved
Ulnar nerve lesion
Median nerve lesion
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1st observe the pattern of wasting
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See if all muscles are weak – those supplied by the ulnar and median nerves. Two muscles are
extremely important
Abductor pollicis brevis - median
Interossei – ulnar
Another important confirmatory sign is to check for sensory loss
If all muscles of the hand are involved follow the table given below
All muscles involved
Site of the lesion
Muscle
Peripheral nerve
T1 root lesion
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Associated features
B/L wasting and fasiculations
(may be slightly asymmetric)
No sensory impairment
Associated bulbar/ pseudobulbar
palsy and UMN signs in the LL
Polyneuropathy
B/L
Associated glove type sensory
loss
Combined ulnar and median
nerve
Sensory loss in the ulnar and
median nerve distributions
Sensory loss in the T1
dermatome
Causes
Motor neuron disease
Causes of polyneuropathy
Cervical spondylosis
Syringomyelia
Cervical rib
Pancoast tumor
If the ulnar nerve is involved further localization is necessary
Ulnar nerve lesion
Site of the lesion
Above the cubital fossa
Features
Flexor carpi ulnaris affected
At the wrist
More clawing (ulnar paradox)
Flexor carpi ulnaris preserved
Causes
Pressure palsy
Trauma
Fracture
Mononeuropathy
Compression in Guyon’s canal
Median nerve lesion
Site of the lesion
Features
Causes
At or above the elbow
At the wrist (commonly in the
carpal tunnel)
Weakness of the flexor
digitorium superficialis and the
lateral half of the flexor
digitorium profundus
Index and middle finger held in
extension
FDS and FDP spared
Palmar cutaneous branch spared
(sensory loss to the center of the
palm. This branch goes above
the flexor retinalculum)
Positive tinel’s test and phallen’s
sign
Claw hand
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Look at the picture given. The following will give a discussion
of how to approach such a case
Where is the lesion?
Site of the lesion
Muscle (MND)
Peripheral nerve
Root (T1)
Associated features
Wasting and fasiculations of all
small muscles of the hand
Weakness of all muscles
B/L involvement
No sensory impairment
Polyneuropathy
Wasting and fasiculations of all
small muscles of the hand
Weakness of all muscles
B/L involvement
Sensory loss in a glove pattern
Ulnar nerve palsy
Weakness of muscles supplied by
the ulnar nerve
Interossei
Note that the abductor pollicis
brevis will be spared (median)
Froment’ s sign +
Sensory loss in the T1 dermatome
Trauma
Fracture
CTS
DM, hypothyroidism
Wrist drop
Where is the lesion?
Site of the lesion
Muscle
Peripheral nerve
Features
Unlikely
C7 root lesion
Polyneuropathy
B/L
Radial nerve palsy
Further localization in radial nerve palsy
Site of the lesion
Features
Lesion above the junction of the Triceps affected
upper and middle thirds of the Brachioradialis affected
humerus
Lesion at the middle 3rd of the Triceps affected
humerus
Brachioradialis spared
Lesion at the wrist
Finger drop only
Triceps and brachioradialis
spared
Causes
Trauma
Fracture
Trauma
Fracture
Trauma
Fracture